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Effects of PACAP administration in the extended amygdala on acoustic startle reflex
Author(s) -
Seiglie Mariel,
Cottone Pietro,
Sabino Valentina
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1265.6
Subject(s) - stria terminalis , acoustic startle reflex , amygdala , endocrinology , medicine , sensitization , septal nuclei , neuropeptide , reflex , central nucleus of the amygdala , antagonist , moro reflex , psychology , neuroscience , receptor
Anxiety‐related disorders are the most common forms of mental disorders; characterized by feelings of excessive worry in the absence of specific external stimuli, they are accompanied by physical, affective and behavioral symptoms. Pituitary adenylate cyclase‐activating polypeptide (PACAP) is a 38‐amino acid peptide expressed not only in the hypothalamus but also in various extra‐hypothalamic regions including the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BNST). PACAP and its receptor PAC1 (PAC1R) have been proposed to play a key role in mediating the behavioral and endocrine responses to stress; however, few studies have examined the involvement of the extrahypothalamic PACAP system in the modulation of stress. Our aim was to elucidate the role of the PACAP/PAC1R system of the CeA and BNST in the context of anxiety‐like behaviors. Acoustic startle response (ASR) is a behavioral test sensitive to states of anxiety and fear. The effects of PACAP bilateral microinfusion into either the CeA or the BNST of male rats on ASR were assessed in this study. In addition, to test the role of the endogenous system, the effects of intra‐CeA and intra‐BNST PACAP antagonist PACAP(6–38) on ASR were assessed, both on basal and on footshock‐induced sensitization of ASR. Infusion of PACAP into both the CeA and BNST increased ASR. Importantly, doses of the antagonist PACAP(6–38) which per se did not affect ASR, were able to prevent the sensitization of ASR induced by footshock, when infused into either the CeA or BNST. These data prove an anxiogenic role for the PACAP/PAC1 system of the extended amygdala and suggest that hyperactivity of this system may underlie the anxiogenic effects of stress. Support or Funding Information NIH grants # MH093650, MH091945, DA030425; T32 grant GM008541